epiglucan and Glucose-Intolerance

Dietary fiber exerts beneficial effects on human health reducing the risk factors of metabolic related diseases such as hyperglycemia, insulin resistance, and hypercholesterolemia. The aim of this study is to demonstrate the efficacy of a food supplement based on brewer's spent grain (BSG) extract in the reduction of postprandial glycemia and insulinemia in normoglycemic subjects. BSG was chemically characterized, revealing the presence of resistant starch (14.64 g/100 g), arabinoxylans (7.50 g/100 g), β-glucans (1.92 g/100 g) and other soluble fibers (6.43 g/100 g), and bioaccessible ferulic acid (91.3 mg/100 g). For the clinical study, 40 normoglycemic subjects were randomized into two groups, 1 and 2 (

Topics: beta-Glucans; Blood Glucose; Cross-Over Studies; Dietary Fiber; Dietary Supplements; Edible Grain; Glucose Intolerance; Humans; Insulin; Insulin Resistance; Postprandial Period; Resistant Starch

Epidemiological studies have shown an inverse relation between a whole grain consumption and risk of type-2 diabetes and cardiovascular disease. One tentative mechanism relates to colonic metabolism of indigestible carbohydrates. In a previous study, we reported a positive relation between colonic fermentation and improved glucose tolerance. This work can be seen as an extension of that study, focusing on the tentative role of specific colonic metabolites, i.e. SCFA. Plasma concentrations of acetate, propionate, and butyrate were determined in the morning in healthy participants (5 women and 10 men, mean ± SD: 25.9 ± 3.2 y, BMI < 25) following 8 different cereal-based evening meals (50 g available starch) varying in content of indigestible carbohydrates. Each participant consumed all test meals in a random order on separate evenings. At a standardized breakfast following evening test meals, the postprandial glucose response (incremental area under the curve, 0-120 min) was inversely related to plasma butyrate (r = -0.26; P < 0.01) and acetate (r = -0.20; P < 0.05) concentrations. Evening meals composed of high-amylose barley kernels or high-β-glucan barley kernels resulted in higher plasma butyrate concentrations the following morning compared with an evening meal with white wheat bread (P < 0.05). The results support the view that cereal products rich in indigestible carbohydrates may improve glucose tolerance through a mechanism involving colonic fermentation and generation of SCFA, where in particular butyric acid may be involved. This mechanism may be one explanation by which whole grain is protective against type 2 diabetes and cardiovascular disease.

Topics: Adult; Amylose; beta-Glucans; Blood Glucose; Butyrates; Cross-Over Studies; Dietary Carbohydrates; Dietary Fiber; Edible Grain; Fatty Acids, Volatile; Feeding Behavior; Female; Glucose Intolerance; Hordeum; Humans; Male; Seeds; Starch; Time Factors; Young Adult

Nonalcoholic steatohepatitis (NASH) is part of the spectrum of nonalcoholic fatty liver disease. However, there are few suitable animal models to study the pathogenesis of NASH or very limited advances in the prevention. Our aims were to establish a mouse model of NASH by intraperitoneally injecting lipopolysaccharide (LPS) at a dose of 1.5 mg per kg body weight per day for 6 weeks and to investigate the potential inhibitory effects of oat β-glucan (1%, 5%, or 10%) added to a specific pathogen-free diet. Intraperitoneal injection of LPS for 6 weeks increased serum LPS levels; decreased serum glucagon-like peptide-2 levels; triggered abnormal aminotransferase activity, glucose intolerance, and insulin resistance; and increased hepatic proinflammatory cytokines (tumor necrosis factor-α, interleukin-6, interleukin-1β), triglyceride, and malonyl dialdehyde levels; but reduced hepatic superoxide dismutase activity. Histologic evaluation revealed evidence of hepatic steatosis, inflammation, and mild necrosis in LPS-treated mice. Dietary supplementation of oat β-glucan prevented most of the LPS-induced metabolic disorders, and improved hepatic steatosis and inflammation, although a dose-dependent effect was not observed. In conclusion, oat β-glucan could inhibit LPS-induced NASH in mice.

Topics: Animals; Avena; beta-Glucans; Disease Models, Animal; Dose-Response Relationship, Drug; Endotoxemia; Fatty Liver; Glucagon-Like Peptide 2; Glucose Intolerance; Inflammation; Insulin Resistance; Interleukin-1beta; Interleukin-6; Lipopolysaccharides; Liver; Male; Malondialdehyde; Mice; Mice, Inbred C57BL; Non-alcoholic Fatty Liver Disease; Oxidative Stress; Superoxide Dismutase; Transaminases; Triglycerides; Tumor Necrosis Factor-alpha; Weight Gain

Salecan is a recently identified water-soluble viscous extracellular β-1,3-D-glucan polysaccharide from an Agrobacterium species. It is a high-molecular-mass polymer (about 2 × 10⁶ Da) and composed of a linear chain of glucosyl residues linked through a repeat unit of seven β-(1,3) and two α-(1,3) glucosidic bonds. In the present study, we examined the effects of dietary Salecan fed at 2 and 5 % in a high-fat diet (64 % energy) in C57BL/6J mice. After 6 weeks, mice fed 2 and 5 % Salecan had significantly lower body weight, fat mass and percentage of body fat mass compared with those fed a high-fat cellulose (control) diet. Both the Salecan groups significantly and dose-dependently improved glucose tolerance, with a 9 and 26 % reduction of glucose AUC, respectively. Liver and adipose tissue weights were also significantly decreased by the Salecan treatment. Supplementation with 5 % Salecan led to lower serum TAG, total cholesterol (TC) and HDL-cholesterol (52, 18 and 19 %, respectively) and lower hepatic TAG by 56 % and TC by 22 % compared with the high-fat cellulose control group. Dietary Salecan intake caused an obvious elevation of fat in the faeces. Supplementation with Salecan disturbed bile acid-promoted emulsification and reduced the size of emulsion droplets in vitro. These results indicate that Salecan decreases fat absorption, improves glucose tolerance and has biologically important, dose-related effects on reducing high-fat diet-induced obesity.

Topics: Adiposity; Animals; Anti-Obesity Agents; beta-Glucans; Cell Size; Diet, High-Fat; Dietary Fats; Dietary Supplements; Emulsifying Agents; Feces; Female; Glucose Intolerance; Intestinal Absorption; Intra-Abdominal Fat; Lipid Metabolism; Liver; Mice; Mice, Inbred C57BL; Obesity; Organ Size; Solubility; Weight Gain

Consumption of a diet high in barley beta-glucan (BG) has been shown to prevent insulin resistance. To investigate the mechanism for the effects of barley BG, three groups of male 7-wk-old C57BL/6J mice were fed high-fat diets containing 0, 2, or 4% of barley BG for 12 wk. The 2% BG and 4% BG groups had significantly lower body weights compared with the 0% BG group. The 4% BG group demonstrated improved glucose tolerance and lower levels of insulin-resistance index and glucose-dependent insulinotropic polypeptide. Consumption of the BG diet decreased hepatic lipid content. Mice on the BG diet also demonstrated decreased fatty acid synthase and increased cholesterol 7alpha-hydroxylase gene expression levels. The BG diet promoted hepatic insulin signaling by decreasing serine phosphorylation of insulin receptor substrate 1 and activating Akt, and it decreased mRNA levels of glucose-6-phosphatase and phosphoenolpyruvate carboxykinase. In summary, consumption of BG reduced weight gain, decreased hepatic lipid accumulation, and improved insulin sensitivity in mice fed a high-fat diet. Insulin signaling enhanced due to the expression changes of glucose and lipid metabolism genes by BG consumption. Consumption of barley BG could be an effective strategy for preventing obesity, insulin resistance, and the metabolic syndrome.

Topics: Animals; beta-Glucans; Body Weight; Dietary Fats; Fatty Liver; Gastric Inhibitory Polypeptide; Gene Expression Regulation, Enzymologic; Glucose Intolerance; Hordeum; Insulin Receptor Substrate Proteins; Insulin Resistance; Lipid Metabolism; Liver; Male; Mice; Mice, Inbred C57BL; Obesity; Phosphorylation; Proto-Oncogene Proteins c-akt; RNA, Messenger; Seeds; Signal Transduction